搜索结果：Pulmonary circulation

Anomalous aortic origin of a pulmonary artery (AORPA), or hemitruncus arteriosus, is a rare congenital anomaly in which one pulmonary artery arises directly from the ascending aorta. Without timely repair, exposure to systemic pressure leads to irreversible pulmonary vascular disease and high early mortality. A 4-month-old female infant presented with failure to thrive, tachypnea, and feeding difficulties. Transthoracic echocardiography and CT angiography confirmed an anomalous right pulmonary artery (RPA) originating from the posterior ascending aorta at the sinotubular junction, with a coexisting patent ductus arteriosus (PDA) and elevated right ventricular pressure. Z-scores for the RPA were not calculated because the vessel was already dilated under systemic pressure. She underwent successful direct end-to-side reimplantation of the RPA into the main pulmonary artery, with ligation of the PDA. The postoperative course was uneventful, and she was discharged on day 5 with improved symptoms. Early surgical correction is critical to prevent pulmonary hypertension and right ventricular overload. Direct tension-free reimplantation is the preferred technique, allowing physiological repair without conduits or patches. Intraoperative assessment confirmed anastomotic patency without residual gradient. Follow-up at 30 days demonstrated a widely patent anastomosis, normalized right ventricular pressure, and satisfactory clinical progress. Structured surveillance is recommended to monitor for restenosis or asymmetric pulmonary artery growth. Prompt diagnosis and surgical repair of AORPA can restore normal pulmonary circulation and prevent irreversible vascular changes. Even in resource-limited settings, careful imaging and meticulous surgical technique yield excellent early outcomes. Long-term follow-up remains essential.

Pulmonary vascular remodeling is implicated in the pathophysiology of pulmonary hypertension (PH) in chronic lung diseases. Computed tomography (CT) metrics of pulmonary vessels may provide insight into the impact of vessel morphology on PH severity in chronic lung diseases (CLD). Are CT-assessed pulmonary vascular abnormalities associated with the presence and severity of PH in chronic obstructive pulmonary disease (COPD) and fibrosing interstitial lung disease (ILD), and how are they related to parenchymal damage? We evaluated 117 patients with CLD (63 with COPD and 54 with ILD), and 38 subjects with idiopathic pulmonary arterial hypertension as a comparator group. Patients with COPD and ILD were stratified according to the presence and severity of PH using right heart catheterization. Pulmonary vessel volumes, stratified in arteries and veins, and the extent of emphysema and fibrosis were assessed by volumetric, non-contrast chest CT scans. Patients with COPD exhibited greater vascular and lung volumes than those with ILD, although they showed lower small-vessel volume when adjusted for lung volume. In both diseases, severe PH was associated with a reduced volume of small arteries normalized to total arterial volume (BV5art/TAV), more pronounced in COPD, who also showed larger central vessel volumes. In COPD, the extent of emphysema did not correlate with either hemodynamic impairment or small-vessel volume. In contrast, in ILD, the extent of fibrosis was unrelated to hemodynamic impairment but was inversely corelated with the volume of small arteries and veins. COPD and fibrosing ILD exhibit marked differences in pulmonary vessel morphology and their relationship with parenchymal remodeling, suggesting distinct mechanisms underlying PH development. In lung disease, the BV5art/TAV ratio appears to be a sensitive marker of hemodynamically confirmed severe PH, particularly in COPD, reflecting intravascular volume redistribution due to peripheral vessel remodeling.

Major aortopulmonary collateral arteries (MAPCAs) are anomalous systemic-to-pulmonary vessels classically associated with complex congenital heart disease. In adults with structurally normal hearts, however, anomalous systemic-to-pulmonary arterial connections represent a broader diagnostic spectrum that includes MAPCA-like vessels, bronchial or non-bronchial systemic arterial collaterals, and isolated systemic arterial supply to normal lung (ISSNL). Aneurysmal degeneration in this setting is uncommon and clinically important because of the risk of rupture or hemorrhage. We report a 48-year-old man presenting with acute non-exertional chest pain. Computed tomography angiography (CTA) demonstrated a 2.6-cm saccular aneurysm arising from a tortuous systemic artery originating from the proximal descending thoracic aorta and extending toward the left lower lobe pulmonary arterial circulation. CTA delineated the vascular origin, course, aneurysmal morphology, and absence of associated congenital cardiac abnormalities. Digital subtraction angiography confirmed a single systemic-to-pulmonary arterial communication. The patient underwent thoracic endovascular aortic repair with adjunctive coil embolization, resulting in complete aneurysm exclusion and symptom resolution. This case highlights an aneurysmal systemic-to-pulmonary arterial connection with MAPCA-like features in a structurally normal adult. The case emphasizes the importance of CTA in differentiating MAPCA-like vessels from bronchial artery aneurysm, non-bronchial systemic collaterals, and ISSNL, and demonstrates the effectiveness of endovascular therapy in excluding a potentially high-risk aneurysmal vascular lesion.

Pulmonary arterial hypertension (PAH) is a rare, progressive pulmonary vascular disorder characterized by pulmonary arteriole remodeling leading to increased pulmonary vascular resistance (PVR). PAH is characterized by vascular pruning and plexiform lesion formation. While these features have been described histologically, a detailed quantitative analysis is lacking. In this study, we used micro-computed tomography (µCT) to provide three-dimensional quantification of pulmonary vascular alterations. We performed µCT imaging on explanted lungs from seven patients with end-stage idiopathic (n=4) or heritable (n=3) PAH and five healthy controls. Arterial lumen diameter, number of acinar vessels, and plexiform lesion distribution were quantified and correlated with clinical and hemodynamic data. We observed a 50% reduction in the diameter of the acinar arterial lumen, and 61% decrease in number of intra-acinar arterioles confirming vascular pruning. Arterial narrowing correlated with PVR and mean pulmonary artery pressure. Heritable PAH showed a higher number of plexiform lesions than idiopathic PAH, with more distal, acinar-level localization. This study provides quantitative evidence of arterial narrowing and objective loss of small intra-acinar arteries in end-stage PAH, supporting their central role in elevated PVR. Pulmonary vascular rarefaction may represent an initiating process of vascular remodeling rather than a secondary phenomenon. Heritable PAH was characterized by a higher number and more distal distribution of plexiform lesions compared to idiopathic PAH, which may contribute to its more severe phenotype.

Pulmonary hypertension (PH) is a progressive, life-threatening disease characterized primarily by pulmonary vascular remodeling in which endothelial dysfunction plays a vital role. However, the molecular factors contributing to this pathological process remain incompletely understood. Through proteomic analysis of hypoxia-treated human pulmonary artery endothelial cells, we identified serine hydroxymethyltransferase 2 (SHMT2) as a potential target in PH, but its role in disease pathogenesis and the underlying mechanisms remain unclear. The expression and function of SHMT2 were assessed in lung samples from patients with PH and in rodent PH models, including hypoxia-exposed mice and monocrotaline- or Sugen 5416/hypoxia-induced rats. Endothelial cell-specific SHMT2 loss and gain of function were achieved by conditional knockout and adeno-associated virus 9-mediated gene modulation. In vitro studies were performed in hypoxia-treated human pulmonary artery endothelial cells and HEK-293T cells. Virtual screening was used to identify a small-molecule inhibitor targeting the nonmetabolic function of SHMT2, and its therapeutic potential was further evaluated in rodent PH models. SHMT2 was upregulated predominantly in pulmonary vascular endothelium of patients with PH and multiple rodent PH models. In vivo, endothelial cell-specific deletion of Shmt2 markedly attenuated pulmonary vascular remodeling and right ventricular dysfunction in PH mice, whereas endothelial cell-specific Shmt2 overexpression aggravated PH development. Consistently, adeno-associated virus 9-mediated endothelial Shmt2 knockdown alleviated PH phenotypes in rat models. Mechanistically, SHMT2 promoted hypoxia-induced endothelial barrier dysfunction mainly through a noncanonical function by blocking the K63-ubiquitin-mediated lysosomal degradation of ras homolog family member B (RhoB). Additional in vivo studies supported an important role of the endothelial SHMT2-RhoB axis in pulmonary vascular remodeling of PH. Through virtual screening, Namodenoson was identified as a small-molecule inhibitor targeting the SHMT2-RhoB pathway. In vivo, Namodenoson showed both preventive and therapeutic effects against PH. This study highlights endothelial SHMT2 as an important contributor to PH pathogenesis and reveals a noncanonical SHMT2-RhoB pathway that promotes endothelial dysfunction. Targeting this pathway may represent a potential therapeutic strategy for PH.

This paper reports a rare adult case of a 64-year-old female with interrupted pulmonary artery in the right middle and lower lobes, complicated by a branch aneurysm at the origin of the right subclavian artery. The patient was admitted for "depressed mood." And she experienced intermittent chest tightness and mild shortness of breath after physical activity. Elevated D-dimer levels were detected, and CT pulmonary angiography confirmed congenital interruption of the right middle and lower lobe pulmonary arteries, accompanied by extensive collateral circulation formation and pulmonary hypertension. This condition originates from abnormal development of the sixth aortic arch during embryogenesis and may clinically mimic chronic pulmonary embolism. Imaging evaluation is central to diagnosis, and treatment requires individualization: asymptomatic patients should undergo conservative follow-up, while those developing hemoptysis or progressive pulmonary hypertension may require interventional embolization or surgical intervention. This case underscores the need for vigilance regarding such rare vascular anomalies, where early recognition and long-term follow-up are crucial for improving patient prognosis.

There are limited data on pharmacologic management of adults living with Fontan circulation. We planned to define changes in pharmacologic management of adults living with Fontan circulation seen at our adult congenital heart disease (ACHD) center and evaluate the association between medication changes and outcomes. We conducted a single center retrospective study. Patient characteristics, cardiac medications, and medication start dates were abstracted by electronic medical record review. Outcomes investigated were new-onset arrhythmia, first time heart failure hospitalization, and transplant-free survival. Outcomes were compared between patients who started medications while under ACHD care with those who did not. The most common cardiac medication class prescribed to patients prior to establishing care was angiotensin converting enzyme inhibitors (ACEi)/angiotensin receptor blockers (ARB) (51.0%), followed by loop diuretics (28.2%) and mineralocorticoid receptor antagonists (MRA) (18.6%). There was a higher incidence of first time heart failure hospitalization and heart transplant or death in patients started on nearly all cardiac medication classes compared to those who were not. Patients started on anti-arrhythmics, loop diuretics, MRA, pulmonary vasodilators, and warfarin had the lowest 5-year transplant-free survival from medication start date. We report commonly utilized cardiac medication classes in adults living with Fontan circulation, with our data suggesting that patients starting anti-arrhythmics, loop diuretics, MRA, pulmonary vasodilators, and warfarin may have decreased 5-year transplant-free survival from medication initiation. These medications were often started in patients with Fontan circulatory failure and/or cirrhosis, suggesting these patients constitute a sicker subset of adults living with Fontan circulation.

Vascular remodeling is a central characteristic of pulmonary hypertension (PH), yet the precise mechanisms underlying this process remain poorly understood. The coimmunoprecipitation assay was used to explore prolyl hydroxylase that modifies BACH1 (BTB and CNC homology 1). Cultured pulmonary artery smooth muscle cells, rodent models with PH, specimens from patients with idiopathic pulmonary arterial hypertension, and single-nucleus RNA sequencing were used to study the role of BACH1 in the regulation of PH and the underlying mechanisms. In this study, we found that the transcription factor BACH1 was upregulated in lung tissues and pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension and animals with experimental PH. Under normoxia, the prolyl hydroxylation of BACH1, mediated by PHD (prolyl hydroxylase) 2, facilitated BACH1 degradation by VHL (von Hippel-Lindau) protein. Hypoxic exposure decreased this prolyl hydroxylation with subsequent increased BACH1 protein stability. The deficiency or overexpression of BACH1 in smooth muscle cells in mice alleviated or exacerbated pulmonary vascular remodeling and hypoxia-induced PH. Hypoxia triggered the accumulation of BACH1 and its recruitment to the promoter region of TGFBR2 (transforming growth factor β receptor type II) in smooth muscle cells. This recrui tment activated TGFBR2 transcription, thereby promoting vascular remodeling by upregulating SMAD (suppressor of mothers against decapentaplegic) signaling and extracellular matrix deposition. Decreased TGFBR2 expression or inhibited kinase activity significantly attenuated the BACH1-induced extracellular matrix genes. Furthermore, the BACH1-enhanced PH development was blunted by a TGFBR2 kinase inhibitor. Our study illustrates that BACH1 is prolyl-hydroxylated in an oxygen/PHD-dependent manner, affecting its stability through VHL. BACH1 is crucial for hypoxia-induced PH by activating TGFBR2/SMAD in smooth muscle cells. Thus, BACH1 inhibition may be a potential therapeutic strategy for PH.

Patients with Fontan circulation represent a high-risk population when facing acute cardiopulmonary decompensation. The use of extracorporeal membrane oxygenation (ECMO) in this patient cohort is rare and technically demanding due to the unique circulatory physiology with passive pulmonary blood flow and predisposition to thromboembolic events. We report the case of a 17-year-old male patient with a history of extracardiac Fontan palliation who developed a life-threatening diffuse pulmonary haemorrhage following blunt chest trauma. The bleeding pattern precluded both interventional and surgical management. Despite initial stabilization attempts, the patient developed progressive respiratory failure refractory to mechanical ventilation, necessitating the initiation of VV-ECMO therapy as a bridge to recovery.Ongoing pulmonary bleeding further complicated the course, precluding the implementation of systemic anticoagulation. Consequently, a heparin-free ECMO strategy was employed. Tailored administration of coagulation factors allowed for the preservation of ECMO circuit patency while maintaining haemostasis. Following gradual respiratory improvement, the patient was successfully weaned from ECMO and discharged without residual organ dysfunction. This case demonstrates the need for personalized ECMO strategies, even in highly challenging haemodynamic scenarios such as Fontan physiology. Favourable outcomes can be achieved when personalized interdisciplinary management is provided in high-volume expert centres for mechanical circulation support (MCS).

Upper gastrointestinal bleeding (UGIB) is a frequent cause of emergency department admission and is most commonly attributed to peptic ulcer disease or portal hypertension-related varices. In critically ill patients, however, pulmonary bleeding may be misinterpreted as hematemesis when blood is swallowed or expelled during retching or airway compromise. In patients undergoing long-term hemodialysis, catheter-related central venous thrombosis can precipitate atypical bleeding presentations. We report the case of a 45-year-old man with chronic kidney disease on maintenance hemodialysis who presented with sudden-onset recurrent hematemesis and hemodynamic instability. Initial evaluation suggested severe UGIB, prompting endotracheal intubation, vasopressor support, and urgent upper endoscopy. Endoscopy demonstrated small esophageal varices and erosive gastropathy without evidence of active bleeding. Subsequent chest computed tomography revealed superior vena cava thrombosis with extensive mediastinal collateral circulation and imaging findings consistent with pulmonary hemorrhage. Bronchoscopy confirmed active bleeding originating from the right bronchial tree, establishing the diagnosis of pulmonary hemorrhage secondary to superior vena cava thrombosis. This case underscores an important diagnostic pitfall: severe pulmonary hemorrhage may mimic UGIB, particularly when initial endoscopic evaluation is non-diagnostic. In hemodialysis patients, superior vena cava thrombosis and collateral vessel formation should be considered as potential mechanisms of airway bleeding even in the absence of classic superior vena cava syndrome. Early thoracic imaging and bronchoscopy are essential when endoscopic findings do not account for persistent or severe hematemesis to prevent diagnostic delays and inappropriate gastrointestinal interventions.

The aim of this study was to analyze the echocardiographic characteristics, intrauterine progression, postnatal outcomes, and follow-up results of fetuses diagnosed with critical pulmonary stenosis with an intact ventricular septum (CPS/IVS) and pulmonary atresia with an intact ventricular septum (PA/IVS) using echocardiography. A retrospective cohort study was conducted on fetuses with isolated PA/IVS and CPS/IVS, collecting both morphological and hemodynamic echocardiographic data and following them postoperatively. A total of 48 cases were included in the study. On the initial ultrasound, eight cases were diagnosed with PA/IVS and 40 cases with CPS/IVS. The right ventricle/left ventricle long axis (RV/LV) ratio, right ventricle long axis (RV-L) z-score, and pulmonary artery/aorta (PA/AO) ratio for PA/IVS were significantly lower than those for CPS/IVS (RV/LV P < 0.001; RV-L P = 0.002; PA/AO P =&#x2009;0.003). Severe tricuspid regurgitation (TR) was predominant in both PA/IVS and CPS/IVS, with six and 28 cases, respectively. A significant increase in RV-L, tricuspid valve (TV) annulus, and pulmonary valve (PV) was observed with gestational age and fetal growth. In an exploratory analysis, earlier gestational age at first ultrasound was associated with neonatal intervention (hypothesis-generating due to small sample size). Post-surgical follow-up showed improvements in RV/LV ratio, tricuspid valve/mitral valve (TV/MV) ratio, and PV z-score (P <&#x2009;0.05), suggesting favorable short-term echocardiographic postoperative outcomes. In this cohort in which all infants achieved biventricular circulation, PA/IVS fetuses showed more compromised RV and PV annular development than CPS/IVS. Serial echocardiography demonstrated measurable growth of RV/TV/PV with gestation, while postnatal and post-intervention follow-up showed improved RV/LV ratio and PV z-scores. These findings support the descriptive value of echocardiography for longitudinal assessment and perioperative follow-up within an integrated management pathway.

Chronic thromboembolic pulmonary hypertension (CTEPH) is rare in adolescents, and evidence regarding balloon pulmonary angioplasty (BPA) in young patients with hereditary thrombophilia remains limited. A 16year-old male was diagnosed with CTEPH and protein S deficiency, characterized by markedly low activity and antigen levels. Genetic analysis revealed a novel PROS1 frameshift variant (c.53del, p.Val18GlyfsTer69) predicted to cause loss of function. Despite anticoagulation and riociguat therapy, pulmonary hypertension persisted, and pulmonary angiography demonstrated predominantly peripheral organized thrombotic lesions. The patient underwent staged BPA at ages 16 and 17, with an additional session at 22. All procedures were completed without complications and were associated with sustained improvement in hemodynamics and exercise capacity during long-term follow-up. This case highlights the importance of considering hereditary thrombophilia in adolescent patients with CTEPH and suggests that staged BPA may be a safe and effective treatment option in selected patients with predominantly peripheral disease.

Pulmonary arterial hypertension (PAH) is a progressive, often fatal disease. Balloon atrial septostomy may relieve symptoms or serve as a bridge to transplant, but carries risks of variable shunting and reocclusion. The atrial flow regulator (AFR) provides a sustained interatrial shunt with a defined shunt size. AFR-Prophet is a prospective, multicenter study evaluating the mechanism of action and safety of AFR in high-risk PAH. Of 32 screened patients, 25 underwent the procedure. The primary end point was serious adverse device effects or procedure-related events at 90 days. Secondary end points included longer-term safety and changes in functional, hemodynamic, and structural parameters. Among 25 patients, 24 received the implant. One patient died prior to implantation because of iatrogenic pericardial tamponade. At 90 days, 7 serious adverse device effects occurred (28%): 3 device-related (oxygen desaturation) and 4 procedure-related. At 3 months, AFR implantation reduced pulmonary vascular resistance and improved cardiac index, despite lower arterial oxygen saturation. Echocardiography showed a smaller right ventricular (RV) end-diastolic diameter and RV/left ventricular ratio, a higher tricuspid annular plane systolic excursion and RV fractional area change, and improved RV-pulmonary artery coupling. Shunt flow was detected in all but 1 patient. NT-proBNP levels decreased, New York Heart Association class improved (>1 class) in 66% of patients, and 6-minute walk distance increased. During the 1-year follow-up, 9 patients died and 3 underwent lung transplantation. Atrial flow regulator therapy in PAH was associated with improved RV function, enhanced RV-pulmonary artery coupling, and better overall cardiac performance. Despite the dismal prognosis of advanced PAH, signals of improved symptoms and physical capacity support interatrial shunting as a potential therapeutic option for carefully selected, even high-risk patients.

Outcomes of venous-arterial extracorporeal membrane oxygenation (VA-ECMO) therapy in acute pulmonary embolism. High-risk pulmonary embolism (PE) has a high mortality risk. VA-ECMO provides essential cardiopulmonary support, although data outcomes remain limited. We sought to describe the characteristics and clinical outcomes of patients supported with VA-ECMO for the management of high-risk PE. We retrospectively analyzed outcomes of adult patients treated with VA-ECMO for high-risk PE at the University of Minnesota between January 2015 and May 2024. High-risk PE was defined by the European Society of Cardiology criteria. Clinical, demographic, procedural, and outcome data were analyzed. Mortality predictors were assessed using logistic regression. Of 1350 patients supported by VA-ECMO, 58 (4.3%) presented with high-risk PE (69% cardiac arrest, 31% shock). Mortality was significantly higher among patients cannulated for cardiac arrest than for shock (72.5% vs. 33.3%, P&#x2009;=&#x2009;0.005). An independent predictor of mortality was out-of-hospital cardiac arrest (OR 6.67, 95% CI 1.15-38.7, P&#x2009;=&#x2009;0.035). The duration of CPR was shorter among survivors (25.9 vs. 44.2&#xa0;min, P&#x2009;=&#x2009;0.02). Neither catheter-directed therapy nor systemic thrombolysis was associated with survival. Major bleeding occurred in 67% of patients and was not significantly associated with mortality. Neurologic injury was the leading cause of death in cardiac arrest patients; multiorgan failure predominated in the shock group. Despite the use of VA-ECMO, mortality in high-risk PE remains elevated, but differed by indication for cannulation. Survival was higher in patients presenting with shock, in-hospital cardiac arrest, shorter CPR duration, and sustained return of spontaneous circulation. Further research is needed to define the role of VA-ECMO and adjunctive therapies across varied clinical presentations.

Gunshot residue (GSR) is an airborne mixture of chemicals and particles released after firearm discharge. There is limited information on cardiopulmonary effects of GSR specifically in a health relevant size fraction. This study evaluates the acute cardiopulmonary effects of GSR (particles &#x2264;2.5&#x202f;&#xb5;m; GSR PM2.5) and investigates the role of the receptor for advanced glycation end-products (RAGE) signaling cascade in the mediation of inflammation and oxidative stress using wild-type (WT) and RAGE knockout (RKO) mice. GSR PM2.5 collected during a law enforcement pistol training contained characteristic GSR markers (lead, copper, and 2,4- dinitrotoluene). Right ventricle measurements were lower in the GSR PM2.5 treated animals compared to the control indicating potential pulmonary vasodilation regardless of genotype. Lead content in the heart was significantly higher in the GSR PM2.5 exposed mice, indicating systemic circulation. Inflammatory markers (NF-&#x3ba;B, TNF-&#x3b1;, SOD-1 and 2) in the lungs of RKO animals were significantly lower compared to the WT groups. The cardiovascular effects, differential inflammatory expression, and influence of RAGE signaling pathway on the cardiorespiratory response to GSR PM2.5 highlight the need for further investigation of longer exposure durations, mechanistic influences, and a more extensive chemical characterization of GSR PM2.5 in toxicological assessments.

Right ventricular (RV) function is a key determinant of outcomes after transcatheter tricuspid interventions. The pulmonary artery pulsatility index (PAPI), an invasive hemodynamic index reflecting RV interaction with filling pressures and pulmonary circulation, has prognostic value in several cardiovascular conditions. However, its role in transcatheter tricuspid valve replacement (TTVR) remains unknown. The aim of this study was to investigate the prognostic implications of PAPI in patients undergoing TTVR. Patients with severe tricuspid regurgitation undergoing orthotopic TTVR with available preprocedural right heart catheterization data were retrospectively analyzed. The primary endpoint was a composite of all-cause mortality and heart failure hospitalization at 2-year follow-up. Patients were stratified according to an optimal PAPI cutoff derived from maximally selected rank statistics on the basis of the log-rank test. Among 94 patients (median age 78 years [Q1-Q3: 72-82 years], 59% women), 28 (30%) had low PAPI (&#x2264;1.13). The median duration of follow-up was 491 days (Q1-Q3: 227-879 days). Kaplan-Meier estimates of survival free from the composite endpoint, all-cause mortality, and heart failure hospitalization were 29.2% (95% CI: 13.6%-62.5%), 52.6% (95% CI: 30.2%-91.7%), and 49.1% (95% CI: 28.4%-85.1%) in the low PAPI group vs 70.0% (95% CI: 58.6%-83.5%), 87.6% (95% CI: 79.2%-96.9%), and 76.6% (95% CI: 65.4%-89.6%) in the high PAPI group (log-rank P < 0.001, log-rank P = 0.006, and log-rank P = 0.017, respectively). On multivariable Cox regression analysis with Firth's penalized likelihood, PAPI &#x2264; 1.13 was independently associated with the primary endpoint (HR: 2.50; 95% CI: 1.18-5.27; P = 0.018), irrespective of RV longitudinal function and age. In patients undergoing TTVR, low preprocedural PAPI identifies a high-risk phenotype, and it is independently associated with adverse outcomes. PAPI may represent a simple and valuable tool for risk stratification in TTVR patients.

Balloon pulmonary angioplasty (BPA) effectively treats chronic thromboembolic pulmonary hypertension (CTEPH); however, its effects on right ventricular (RV) remodeling remains unclear. This study investigates RV reverse remodeling patterns and key hemodynamic determinants in patients undergoing sequential BPA therapy. In this retrospective study, 46 patients who underwent BPA at monthly intervals were included. Serial echocardiography was used to monitor cardiac structure and function, while right heart catheterization assessed hemodynamic parameters before and after treatment. Longitudinal changes were analyzed using mixed-effects models with piecewise assessment of early and late treatment phases. Significant improvements in right ventricular structure and function were observed across BPA sessions. Notably, right atrial transverse diameter and tricuspid annular systolic velocity demonstrated early responses to BPA, with significant changes evident during the initial treatment phase. In longitudinal analyses, early treatment phases (baseline to BPA3) were characterized by marked reverse remodeling, including reductions in right atrial area (RAA), RV end-diastolic transverse diameter, and wall thickness, accompanied by improvements in tricuspid annular plane systolic excursion, enhanced RV function. Greater reductions in pulmonary vascular resistance (PVR) were associated with more pronounced RV reverse remodeling, particularly in RAA. A temporal pattern of RV reverse remodeling is observed during serial BPA, characterized by substantial early improvements followed by a plateau in later sessions. These changes are closely associated with reductions in PVR, supporting a central role of afterload reduction in driving RV recovery. This pattern may help inform the optimization of BPA treatment strategies.

High-risk pulmonary embolism (PE), defined as PE causing hemodynamic instability, remains associated with high acute mortality and currently warrants acute treatment with systemic thrombolysis. Mechanical thrombectomy can be considered where thrombolysis is inappropriate, as an alternative, or in addition to, but more prospective data are needed. This analysis evaluates the safety, effectiveness, functional, and quality of life (QoL) outcomes in high-risk PE patients who were treated using mechanical thrombectomy with computer-assisted vacuum thrombectomy (CAVT) devices. Among the first 595 patients enrolled in the prospective, international STRIKE-PE study, 48 were identified as having high-risk PE. Outcomes included change in right-to-left ventricular ratio from baseline to 48-hour follow-up, 48-hour composite major adverse events (MAE), additional safety end points, and 90-day changes in functional and QoL assessments. Mean right-to-left ventricular ratio decreased from 1.50 &#xb1; 0.36 to 1.02 &#xb1; 0.18 (P < .001). One study-defined MAE (major bleeding) occurred. One all-cause mortality and 1 symptomatic PE recurrence occurred within 30 days. Borg scale at rest improved from baseline to discharge (P < .001) and discharge to 90 days (P = .045). Borg scale after 6-minute walk test, 6-minute walk test distance, EQ-5D-5L index value, EuroQoL Visual Analog Scale, and Pulmonary Embolism QoL score improved (all P < .001). New York Heart Association class returned to pre-PE baseline. Six patients received systemic thrombolysis (1 periprocedure and 5 postprocedure); majority of patients received none. CAVT for high-risk PE was feasible and associated with a low incidence of MAE and a low 30-day mortality rate. CAVT treatment facilitated improvements in hemodynamic status and RV strain. Dyspnea, distance walked, functional status, and QoL significantly improved.

Catheter-directed thrombolysis (CDL) and mechanical thrombectomy (MT) are increasingly used for intermediate-high-risk pulmonary embolism (PE), yet comparative long-term outcomes remain uncertain. We aimed to compare the effectiveness and safety of CDL versus MT in real-world clinical practice. Using the multi-institutional TriNetX network, we identified adults with acute intermediate-high-risk PE treated with CDL or MT. One-to-one propensity score matching was performed across demographics, comorbidities, and laboratory variables. Outcomes were assessed up to 2 years post-index. The primary outcome was all-cause mortality, while secondary outcomes included hospitalization, major adverse cardiovascular events (MACE), pulmonary hypertension (PH), and bleeding. After matching, 1290 patients remained in each group with balanced baseline characteristics, with a median follow-up of approximately 1.5 years. Long-term mortality was similar between CDL and MT (3.1% vs. 3.5%; p&#x2009;=&#x2009;0.061). MACE rates were comparable (5.2% vs. 4.6%; p&#x2009;=&#x2009;0.933), with no significant difference in PH (3.0% vs. 3.24%; p&#x2009;=&#x2009;0.352). CDL was associated with higher hospitalization rates (2.2% vs. 0.9%; p&#x2009;=&#x2009;0.026), while bleeding events were low and similar between groups. In this large real-world cohort of patients with intermediate-high-risk PE, CDL and MT demonstrated broadly comparable long-term outcomes, suggesting no clear superiority of either strategy and supporting ongoing clinical equipoise. Ongoing randomized trials are needed to further inform optimal management.